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Protective effects of scoparone against lipopolysaccharide-induced acute lung injury.

Abstract
The purpose of this study was to investigate the protective effects and molecular mechanisms of scoparone on lipopolysaccharide (LPS)-induced acute lung injury in mice. Mice model of acute lung injury (ALI), induced by intranasal instillation of LPS, was used to investigate the protective effects of scoparone in vivo. The alveolar macrophages were used to investigate the molecular mechanisms of scoparone in vitro. The results showed that scoparone treatment remarkably attenuated LPS-induced pulmonary edema, histological severities, myeloperoxidase activity, and TNF-α, IL-6 and IL-1β production in vivo. We also found that scoparone inhibited LPS-induced TLR4 expression, NF-κB activation, TNF-α, IL-6 and IL-1β production in alveolar macrophages in vitro. In conclusion, our results suggest that scoparone has a protective effect on LPS-induced ALI via suppression of TLR4-mediated NF-κB signaling pathways.
AuthorsNiu Niu, Baolan Li, Ying Hu, Xuebing Li, Jie Li, Haiqing Zhang
JournalInternational immunopharmacology (Int Immunopharmacol) Vol. 23 Issue 1 Pg. 127-33 (Nov 2014) ISSN: 1878-1705 [Electronic] Netherlands
PMID25151099 (Publication Type: Journal Article)
CopyrightCopyright © 2014 Elsevier B.V. All rights reserved.
Chemical References
  • Anti-Inflammatory Agents, Non-Steroidal
  • Coumarins
  • Cytokines
  • Lipopolysaccharides
  • NF-kappa B
  • Toll-Like Receptor 4
  • Peroxidase
  • scoparone
Topics
  • Acute Lung Injury (chemically induced, prevention & control)
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal (administration & dosage)
  • Artemisia (immunology)
  • Cells, Cultured
  • Coumarins (administration & dosage)
  • Cytokines (genetics, metabolism)
  • Disease Models, Animal
  • Gene Expression Regulation (drug effects)
  • Humans
  • Lipopolysaccharides (metabolism)
  • Macrophages, Alveolar (drug effects, physiology)
  • Male
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B (metabolism)
  • Peroxidase (metabolism)
  • Pulmonary Edema (chemically induced, prevention & control)
  • Signal Transduction (drug effects)
  • Toll-Like Receptor 4 (genetics, metabolism)

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